Alzheimer's

• Adults with a father who had Alzheimer’s showed greater tau buildup, a key marker of the disease.

• Women in the study had more widespread tau in their brains than men.

• Findings could help guide personalized prevention strategies before memory loss begins.

We’ve all heard how having a parent with Alzheimer’s could bump up our own risk of developing the disease — but what if it matters which parent? 

A recent study by the American Academy of Neurology reveals something surprising: it might actually be your dad’s history, not your mom’s, that correlates more strongly with a specific Alzheimer’s marker in the brain. While previous research often pointed to maternal inheritance, this study flips the narrative, focusing on how tau protein — not just memory decline — might have its own “family story.”

“We were surprised to see that people with a father with Alzheimer’s were more vulnerable to the spread of tau in the brain, as we had hypothesized that we would see more brain changes in people with affected mothers,” study author Sylvia Villeneuve, Ph.D. said in a news release. 

The study

Researchers tracked 243 cognitively healthy adults, all around 68 years old, who had at least one parent (or two siblings) with Alzheimer’s. Importantly, none of the participants had any thinking or memory issues when the study began. 

They underwent brain scans and memory testing, then were followed for almost seven years. Over that time, 71 people developed mild cognitive impairment — often seen as an early step toward Alzheimer’s. 

The team measured two key protein markers in the brain: beta-amyloid and tau. Tau buildup is especially linked to Alzheimer’s disease.

The results

The researchers discovered a paternal pattern throughout the study. 

Participants whose fathers had Alzheimer’s showed a greater spread of the tau protein in their brains. This was a surprising finding— especially since the team expected maternal influence to be stronger. 

Additionally, gender mattered too. Women in the study had a heavier tau buildup than men — and were more likely to show widespread tau protein spread.

It’s important to note that these findings are associations, not proof of direct cause. Additionally, the study participants were mostly white, so the findings may not apply equally across all races and ethnicities.

However, the researchers explained that these insights might help health care professionals design personalized interventions that protect those at higher risk before symptoms even surface.

“Better understanding these vulnerabilities could help us design personalized interventions to help protect against Alzheimer’s disease,” Dr. Villeneuve said.

• A shingles vaccine was tied to a 20% drop in new dementia cases over seven years.

• The U.K. rollout created a natural experiment using birthdate eligibility.

• Reduction was especially strong in women, beyond the effects on shingles itself.

Researchers at Stanford Medicine dove into health records from older adults in Wales to explore the link between the shingles vaccine and the risk of dementia. 

They focused on those eligible for the live-attenuated shingles vaccine (Zostavax) based on an exact birthdate cutoff: anyone born on or after September 2, 1933 was eligible, while those born just before weren’t. 

Because both groups were nearly identical in age, health, and behavior — except for vaccine eligibility — this setup acted like a “natural randomized trial.” 

The result? Receiving the shingles vaccine was associated with a 20% lower chance of developing dementia over the next seven years, even after accounting for who actually got vaccinated.

“All these associational studies suffer from the basic problem that people who get vaccinated have different health behaviors than those who don’t,” researcher Pascal Geldsetzer, M.D., Ph.D., said in a news release. “In general, they’re seen as not being solid enough evidence to make any recommendations on.”

The study

For the study, the researchers used a regression discontinuity design — it allows them to compare people who are alike except for being eligible for vaccination. By looking at those born just before and after the September 1933 cutoff, they ensured both groups were very similar. One group had a 47.2% vaccination rate, while the other had only 0.01%.

Health records were tracked for seven years, noting new dementia diagnoses. To make sure the vaccine itself was the key difference, they checked that the groups didn’t differ in other diseases, doctor visits, or preventive health behavior. They even used alternative analyses to confirm the findings held up no matter how they looked at the data .

The study

The researchers found that there were fewer dementia cases overall. Being eligible for the vaccine cut new dementia diagnoses by 1.3 percentage points, or about 8.5% fewer cases.

In participants who actually got the shot, the reduction jumped to 3.5 points, a 20% drop in dementia risk.

“It was a really striking finding,” Dr. Geldsetzer said in the news release. “This huge protective signal was there, any which way you looked at the data.”

The team also learned that women had greater protective cognitive benefits than men. Though the vaccine lowered dementia risk for both sexes, the effect was significantly stronger in women.

What this means for you

The findings highlight a bonus to getting your shingles vaccine: the potential to protect your brain. Scientists are still trying to figure out why it works — whether it’s because the vaccine stops inflammation-causing shingles outbreaks, or if the vaccine primes the immune system in a way that wards off dementia.

While the study is robust, with careful methods that reduce bias, it’s still observational. That means it can show a strong connection, but not absolute proof. The researchers stress the need for randomized clinical trials before making firm claims. 

• UCLA Health researchers mapped four distinct pathways leading to Alzheimer’s disease using electronic health records.
  

• The findings suggest that tracking diagnostic sequences predicts Alzheimer’s risk better than analyzing isolated conditions.
  

• The study, validated with a nationally representative cohort, could transform early detection, personalized prevention, and intervention strategies.

Who is most at risk of developing Alzheimer’s disease? If doctors knew the definitive answer, it might lead to earlier treatment and diagnosis. Researchers at UCLA may have uncovered some helpful clues.

Writing in the journal eBioMedicine, the researchers at UCLA Health said they have identified four unique diagnostic pathways that can lead to Alzheimer's disease, offering a more nuanced understanding of how the neurodegenerative condition develops over time. 

By analyzing electronic health records from nearly 25,000 patients, the study sheds light on how specific sequences of medical conditions – not just individual risk factors – can influence a person’s likelihood of developing Alzheimer’s. The research marks a significant departure from traditional approaches that focus on isolated risk conditions. 

Instead, UCLA scientists mapped the step-by-step clinical trajectories that precede an Alzheimer’s diagnosis, offering new tools for early detection and prevention.

Patterns, not just risk factors

“We found that multi-step trajectories can indicate greater risk factors for Alzheimer’s disease than single conditions,” said first author Mingzhou Fu, a medical informatics pre-doctoral student at UCLA. “Understanding these pathways could fundamentally change how we approach early detection and prevention.”

The study identified four primary diagnostic trajectories:

1. Mental Health Pathway – Psychiatric conditions such as depression or anxiety that eventually lead to cognitive decline

2. Encephalopathy Pathway – Disorders involving brain dysfunction that worsen progressively

3. Mild Cognitive Impairment Pathway – A gradual decline in memory and cognitive functions, often preceding Alzheimer's
   

4. Vascular Disease Pathway – Cardiovascular conditions like hypertension that heighten the risk of dementia
   

Each pathway was linked with distinct demographic and clinical features, suggesting that different subgroups of the population may be predisposed to different disease routes.

Chronology of conditions

The researchers found that 26% of all diagnostic sequences showed a consistent, directional order. For instance, patients with hypertension frequently developed depressive episodes before being diagnosed with Alzheimer’s. These patterns, according to the team, may be key to identifying at-risk patients earlier in their disease progression.

“Recognizing these sequential patterns rather than focusing on diagnoses in isolation may help clinicians improve Alzheimer’s disease diagnosis,” said Dr. Timothy Chang, the study’s senior author and assistant professor of Neurology at UCLA Health.

The team validated their findings using the All of Us Research Program, a diverse and nationally representative database. The confirmation of these patterns across a wide population enhances the study’s relevance and applicability to clinical practice nationwide.

The study concluded that the innovative use of longitudinal electronic health data signals a promising shift in Alzheimer’s research, moving toward predictive and personalized care models that could significantly improve patient outcomes.

• A new study links prolonged sedentary behavior to increased risk of cognitive decline and brain shrinkage associated with Alzheimer’s disease.

• Even daily exercise does not offset the negative impact of extended sitting, especially in individuals with a genetic predisposition to Alzheimer’s.

• Researchers emphasize the importance of reducing total sitting time as a strategy to support brain health in aging adults.

Studies from a decade ago suggested “sitting is the new smoking,” suggesting that a sedentary lifestyle was bad for your health. Now, a new study from Vanderbilt University Medical Center and the University of Pittsburgh reveals that spending too much time sitting, even for those who exercise regularly, can significantly increase the risk of cognitive decline and brain shrinkage associated with Alzheimer’s disease.

Published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, the research explores the effects of sedentary behavior in aging adults and its link to neurodegeneration. The findings carry serious implications for the more than six million Americans living with Alzheimer’s and the millions more at risk.

Tracking movement, measuring impact

Admittedly, it was a small sample. The research, led by Dr. Marissa Gogniat, assistant professor of Neurology at the University of Pittsburgh, involved 404 adults aged 50 and older.

Participants wore activity-tracking devices for a week, providing detailed data on how much time they spent sitting or lying down. The researchers then analyzed this sedentary behavior against cognitive tests and brain imaging over a seven-year period.

The results were clear: individuals who were more sedentary experienced greater cognitive decline and notable shrinkage in brain regions critical for memory and Alzheimer’s development. These effects were observed regardless of participants’ exercise routines.

Genetic risk increases the threat

The study found that individuals carrying the APOE-e4 allele—a known genetic marker for Alzheimer’s disease—were particularly susceptible to the negative effects of sedentary behavior. This suggests that lifestyle modifications may be especially vital for those with an elevated genetic risk.

“Reducing your risk for Alzheimer’s disease is not just about working out once a day,” Gogniat said. “Minimizing the time spent sitting, even if you do exercise daily, reduces the likelihood of developing Alzheimer’s disease.”

The research was supported by the Alzheimer’s Association and the National Institute on Aging and adds to a growing body of evidence that daily habits—beyond structured workouts—play a pivotal role in long-term cognitive health.